To investigate the role of autonomic reflexes in stroke-work optimization, we studied ventriculoarterial coupling in unanesthetized dogs with the autonomic system intact and blocked. Ventricular contractility was quantified by the slope of the end-systolic pressure-volume relation, ventricular elastance (E(es)). Arterial system properties were quantified by the ratio of end-systolic pressure to stroke volume, arterial elastance (E(a)). The coupling between left ventricle and arterial system was expressed by the E(a)-to-E(es) ratio. Changes in arterial blood pressure during nitroprusside or angiotensin II infusion were used to elicit reflex-mediated influences on ventriculoarterial coupling. With the autonomic system intact, E(es) doubled during nitroprusside infusion while E(a) remained unchanged due to reactive vasoconstrictor forces and tachycardia. Consequently, the E(a)-to-E(es) ratio fell 50% from baseline. Angiotensin II infusion increased E(a) 46% but did not significantly change E(es), resulting in a 26% increase in the E(a)-to-E(es) ratio. In contrast to ventriculoarterial coupling, stroke work was insensitive to changes in afterload, remaining close to its theoretical maximum. After autonomic blockade, E(es) tended to decrease during nitroprusside and increased during angiotensin II infusion in parallel with changes in E(a), so that the E(a)-to- E(es) ratio did not change from baseline as much as it did with the autonomic system intact. Again, the left ventricle maintained nearly 90% of its maximal stroke work. Thus, over a wide range of afterload, stroke work was kept near its theoretical maximum, independent of autonomic neural regulation. These findings suggest that the feedback neural regulation to restore normal arterial pressure could augment the variability of ventriculoarterial coupling condition when vascular responsiveness to the baroreflexes is limited by vasoactive agents.
